Ionizing radiation occurs not only during nuclear and radiological terrorist attacks or nuclear accidents but also in medical applications and daily life. In recent years, the potential toxic effects of low-dose ionizing radiation on the male reproductive system have raised public health concerns. Most specifically, for the testis, a highly sensitive target organ to ionizing radiation, there is an urgent need to determine the mechanisms underlying the association between radiation-induced spermatogenic failure and male infertility. Focusing on the potential injurious effects of low-dose ionizing radiation on spermatogenesis, this review presents a summary and analysis of various underlying mechanisms including oxidative stress, apoptosis, and DNA damage repair and reviews recent domestic and international strategies for protecting against radiation-induced reproductive system damage in order to offer references for future research on the injurious effects of low-dose radiation on spermatogenesis and relevant protection.

Objective To compare the changes in biological indicators of human corneal epithe-lial(HCET)cells and rabbit corneas after exposure to different doses of ultraviolet B(UVB)radia-tion,so as to evaluate the impact of UVB radiation on corneal injury effects.Methods In cell exper-iment,HCET cells were divided into groups with radiation doses of 0,6,12,18,and 24 mJ/cm2.The effect of UVB radiation on HCET cell viability was detected using the CCK-8 assay,and the level of intracellular DNA damage was assessed by immunofluorescence.In the animal experiment,15 healthy New Zealand white rabbits(30 eyes)were randomly divided into groups with radiation doses of 0,1.35,2.16,4.32,and 6.48 J/cm2.The UVB exposure time for the radiation groups was 30 minutes per day for 3 consecutive days.Corneal injury was evaluated using methods such as slit-lamp microscopy,sodium fluorescein staining,central corneal thickness measurement,optical coherence tomography(OCT)imaging,and hematoxylin and eosin(HE)staining.Results Compared with the control group,cell viability in the radiation groups gradually decreased,and the level of DNA damage gradually increased with increasing radiation dose.As the radiation dose increased in the radiation groups,the degree of corneal opacity in rabbits gradually worsened,the central corneal area gradu-ally thickened,and OCT revealed high-intensity scattered light signals with the formation of shadow areas.Results from HE staining,immunohistochemistry,Western blot(WB),and sodium fluores-cein staining showed that the 1.35 J/cm2 group caused mild corneal injury,with damage reaching the corneal epithelial layer.In the 2.16 J/cm2 group,the corneal injury presented as dense punctate distribution,with damage extending from the epithelial layer to the superficial stroma.The number of ephrin type-A receptor 2(EphA2)protein-stained cells was relatively small,and the staining was light,showing a weak positive result.In the 4.32 J/cm2 and 6.48 J/cm2 groups,the corneal injury was irreversible,with damage gradually progressing from the corneal epithelial layer and superficial stroma to the endothelial layer.The number of EphA2 protein-stained cells was relatively large,and the staining was dark,showing a strong positive result.Conclusion This study comprehensively e-valuates the dose-dependent injury effects of UVB on HCET cells and New Zealand white rabbit cor-neas through cell and animal experiments.It elucidates that UVB radiation could induce corneal cell DNA damage,promote inflammatory responses,and trigger apoptosis by upregulating γ-phosphoryla-ted histone H2AX(γH2AX)and EphA2.The self-repair ability and process of corneal injury are preliminarily explored,providing a basis for further research on mechanisms of corneal injury caused by ultraviolet radiation and the development of protective drugs.

High intensity ultraviolet radiation exists in special military operation environments such as oceans,plateaus,polar regions and deserts,which is a leading contributor to eye damage and can lead to luminous keratitis,dry eyes,pterygium,cataract and macular degeneration.Ultraviolet radiation can cause acute and chronic injury to eyes by inducing DNA damage,oxidative stress and inflammatory reaction.The commonly used clinical drugs have played a role in relieving symptoms and promoting the repair of ocular tissues,but there are still limitations.The research on targeted therapeutic drugs,proteins and their derived peptides,vitamins and their coenzymes,as well as natural active ingredients of animals and plants has provided new ideas for the development of more effective drugs that can protect eyes from ultraviolet and for medical support to China's army in special environments.Based on the literature currently available,this paper reviews the eye injury caused by ultraviolet radiation and therapeutic drugs in terms of types of eye diseases,injury mechanisms,treatment strategies and drug development.

Ionizing radiation occurs not only during nuclear and radiological terrorist attacks or nuclear accidents but also in medical applications and daily life. In recent years, the potential toxic effects of low-dose ionizing radiation on the male reproductive system have raised public health concerns. Most specifically, for the testis, a highly sensitive target organ to ionizing radiation, there is an urgent need to determine the mechanisms underlying the association between radiation-induced spermatogenic failure and male infertility. Focusing on the potential injurious effects of low-dose ionizing radiation on spermatogenesis, this review presents a summary and analysis of various underlying mechanisms including oxidative stress, apoptosis, and DNA damage repair and reviews recent domestic and international strategies for protecting against radiation-induced reproductive system damage in order to offer references for future research on the injurious effects of low-dose radiation on spermatogenesis and relevant protection.

Objective:To investigate the impact of diabetes mellitus (DM) and stroke on long-term outcomes in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI).Methods:Total 411 consecutive ACS patients undergoing PCI at the Ninth People′s Hospital of Zhengzhou between December 2014 and June 2018 were recruited, including 319 males and 92 females with a mean age of (64.7±10.1) years. These patients were divided into 4 groups according to the presence or absence of history of diabetes or stroke: non-DM non-stroke group ( n=192) , DM group ( n=140), stroke group ( n=41), and DM+stroke group ( n=38). The data of baseline demographic characteristics, clinical feature, coronary angiographic findings, and cardiovascular adverse events during long-term follow-up were obtained. Kaplan-Meier curves were used to investigate the long-term clinical outcomes among groups. Results:The mean interval of follow-up was (24.1±13.8) months. Patients with DM+stroke had the highest rates of non-fetal myocardial infarction (χ 2=24.932) , non-fetal stroke (χ 2=9.434) , hospitalization due to heart failure/angina (χ 2=69.290) , revascularization (χ 2=22.918) , cardiovascular death(χ 2=13.473)and all-cause death(χ 2=17.724)as well as hard endpoint events (the sum of non-fetal myocardial infarction, non-fetal stroke, and all-cause death) (χ 2=30.268)and combined major adverse cardiovascular events (MACE) (the sum of hard endpoint events, hospitalization due to heart failure/angina, and revascularization) (χ 2=119.556)among 4 groups(all P<0.01). In Kaplan-Meier survival analysis, the cumulative ratio of freedom from all-cause death decreased significantly in DM+stroke group compared with no DM no stroke group ( HR=17.121, 95 %CI: 2.527-115.934, P<0.01), but no statistical difference was observed in the cumulative ratio of freedom from all-cause death between DM+stroke group and DM group or stroke group respectively ( HR=3.178, 95 %CI: 0.744-13.582; HR=1.383, 95 %CI: 0.374-5.118; all P>0.05) . Meanwhile, patients with DM+stroke presented significantly lower cumulated ratio free from combined MACE than patients with non-DM non-stroke ( HR=5.423, 95 %CI:2.941-10.036, P<0.01), and the cumulated ratio free from combined MACE also decreased significantly in DM+stroke group as compared to DM group or stroke group respectively ( HR=1.859,95 %CI: 1.167-2.962; HR=1.991,95 %CI: 1.178-3.364; all P<0.01) . Conclusions:ACS patients with combined history of DM and stroke have a worse long-term outcomes after PCI than those with DM alone or stroke alone or without DM or stroke. DM and stroke seemed to have an additive effect on decrease in the cumulative ratio free from combined MACE in ACS patients following PCI.